The cells that make us fat discovered: these are triggered by inflammation


For many years, we heard that the single reason why we put on weight is the increase in calories intake, while eating fewer calories means instead losing weight.

Today we know that this is not always true and that food-related inflammation may be amongst the most relevant causes for putting on weight in certain conditions, independently from the calories intake.

Strenuous and lengthy intellectual conflicts have been caused by the idea that a specific food might have weight-loss or weight-gain powers irrespective of the energetic content, in particular if referred to the now-obsolete concept of food intolerances. Whoever loses weight by undertaking a diet centred on the tight control of one or more Great Food Clusters knows this very well, but the scientific explanation has become clearer only in the last few years.

In 2012 I had the honour to take part to the meeting on food intolerances organized by “Corriere della Sera” (one of the major Italian daily newspapers); here, the discussion centred on food-triggered inflammation and its revolutionary concept, even though the correlation between food reaction and weight-gaining had already been described by important pieces of research by studying the role of certain cytokines and immune cells of the adipose tissue, called macrophages.

A study conducted by a group of Viennese endocrinologists, published on the International Journal of Obesity (Zeyda M et al, Int J Obes (Lond) 2007 Jun 26; [Epub ahead of print]), shed new light on the triggers of weight-gain and its correlation with low-grade inflammation. Thanks to these results, it is today even clearer why people showing food-related inflammation may develop insulin resistance more easily.

Zeyda et al. Work is not the sole one: since 2004, Mitchell Lazar has published on Science data showing why macrophages may produce resistin as a simple response to low-grade inflammation and cause insulin-resistance and fat accumulation in adipose cells as a defensive response.

By demonstrating how BAFF, a cytokine deeply linked to food-related inflammation, leads directly to situations of insulin resistance, various other articles have finally identified the bridge from inflammation to weight-gain, as well as to the stimulation of adipokines that lead to obesity.

Clearly, a diet able to control food-related inflammatory events (intolerances) may help recover one’s own ideal weight, reducing the fat body mass and increasing the lean body mass.

It is clear that an intoxicated and inflamed organism has the tendency to gain weight, and why people with food allergies often put on weight without understanding the reasons behind it.

The key to understand these phenomena stands in the production of inflammatory cytokines (like BAFF, for example) and in the activation of those macrophages residing into the adipose tissue, usually known for their anti-inflammatory role but in reality also able to drive pro-inflammatory cytokines production and lead to insulin resistance, if negatively affected by diet and low-grade inflammation.

In other words, these cells can lay the foundations to conditions similar to those present in diabetes, facilitating the fat body mass increase.

Today we can measure the level of inflammatory cytokines within the organism and starting from this we can understand the level of on-going inflammation. We can follow the inflammatory trend along the course of a diet and of a supportive therapy, aimed at reducing the insulin resistance.

Some of such measurements are included within the food inflammation evaluating test, which already allows us to understand every “personal nutritional profile” and to set the most suitable regime to achieve the ideal weight.

In our Milan centre (SMA), we have been following, for many years, patients with food-related inflammation and with the need for losing fat body mass, by providing a tailored therapeutic pathway to help and accompany the person towards healing and regaining the best shape.